Annals of Tropical Medicine and Public Health
Home About us Ahead Of Print Instructions Submission Subscribe Advertise Contact e-Alerts Editorial Board Login 
Users Online:2976
  Print this page  Email this page Small font sizeDefault font sizeIncrease font size
 


 
Table of Contents   
CASE REPORT  
Year : 2013  |  Volume : 6  |  Issue : 2  |  Page : 245-247
Invasive aspergillosis in a HIV patient on prolonged steroid therapy


Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India

Click here for correspondence address and email

Date of Web Publication14-Aug-2013
 

   Abstract 

Central Nervous System complications are the most dreaded complications in patients of HIV. CNS aspergillosis in HIV is a rare complication. The primary risk-factors for invasive aspergillosis are profound neutropenia and glucocorticoid use; risk increases with longer duration of these conditions. In our case report, the HIV patient was treated with Anti Tubercular Treatment and steroids for CNS tuberculosis previously. Use of steroids might have predisposed him for aspergillosis. Physicians should be aware that the CNS might be the only site of Aspergillus involvement and should include CNS aspergillosis in the differential diagnosis of HIV-infected patients presenting with focal neurologic signs and symptoms, especially, when the head Computed Tomography reveals hypodense lesions.

Keywords: CNS aspergillosis, HIV, neutropenia, steroid use

How to cite this article:
Reddy H, Saraf S, Singh MM. Invasive aspergillosis in a HIV patient on prolonged steroid therapy. Ann Trop Med Public Health 2013;6:245-7

How to cite this URL:
Reddy H, Saraf S, Singh MM. Invasive aspergillosis in a HIV patient on prolonged steroid therapy. Ann Trop Med Public Health [serial online] 2013 [cited 2019 Sep 23];6:245-7. Available from: http://www.atmph.org/text.asp?2013/6/2/245/116493

   Introduction Top


CNS complications are the most dreaded complications in patients of HIV. CNS aspergillosis in HIV is a rare complication. Case reports of CNS aspergillosis in a HIV patient are rare. The authors report a rare case of CNS aspergillosis in a HIV patient presenting with headache and vomiting along with mild to moderate grade fever followed by altered sensorium. No neurological deficit was detected. He was treated with ATT and steroids for CNS tuberculosis previously. Use of steroids might have predisposed him for aspergillosis.


   Case Report Top


A 30-year-old male presented to our department on 12 January 2010 with a 25 days history of moderate grade fever, headache, along with generalized weakness. Physical examination revealed glasgow coma scale of 10/15, a temperature of 39.2°C, a blood pressure of 110/70 mm Hg, a pulse rate of 76/min, and a respiratory rate of 22/min. No neurological deficit was detected. Even after taking antibiotics and paracetamol, there was no improvement, later on the basis of chest X-ray he was diagnosed pulmonary tuberculosis for which he took anti-tubercular treatment for 5 months (standard five drug regimen).

By the end of June 2010 patient started having oral ulcers and episodes of loose stools, then he was diagnosed to be HIV reactive. He was put on anti-retroviral therapy (stavudine-lamivudine-efavirenz) regimen.

Subsequently, a month later he started having headache, generalized tonic seizures, followed by left sided hemiparesis.

Again he was admitted from 23/7/10 to 16/8/10. Then, Cerebro Spinal Fluid analysis was done which revealed Total Leucocyte Count-30 cells Differential Leucocyte Count -Neutrophils 15 Lymphocytes 85 , protein-516, Adenosine Deaminase -46.5, India Ink-negative, Cryptococcal antigen positive.



Considering his raised ADA and Cryptococcal antigen positive and positive HIV status, he was given both anti-tubercular treatment (T. Isoniazid 300 mg, T. Ethambutol 800 mg, T. Levofloxacin 750 mg, Note: patient showed rifampicin induced hepatitis) and added amphotericin-B. His CD-4 count (9/8/10) was 126. CT scan was within normal limits. On discharge (16/8/10), his power was 4/5 in both left upper and lower limb, which gradually improved in 2 months.

Again after 6 months, he was admitted (10/12/10-17/12/10) with the complaints of mild to moderate fever along with headache for 7 days. On admission, his CSF analysis was again repeated (TLC-80, DLC-N 20 L 80 , protein-108.1 mg/dl sugar-25, India Ink-negative, CSF Venereal Disease Research Laboratory-negative). After 7 days of admission he was discharged on T. Isoniazid 300 mg, T. Pyrizinamide 1000 mg, T. Levofloxacin 750 mg. CT head was not done. His ATT was stopped in early February 2011.

In the middle of August 2011, patient developed headache and vomiting along with mild to moderate grade fever for 10 days followed by altered sensorium for the past 4 days. CT Head was done, which revealed non-communicating hydrocephalus with obstruction at the level of 3 rd ventricle but there were no sign of raised Intra cranial tension. CSF analysis was done (TLC-70, DLC-N 10 L 90 , protein-760, sugar-8, India Ink-negative, ADA-14.7). ATT was started again, 10 days after treatment CSF analysis was repeated which revealed TLC-28, DLC-N 97 L 3 , protein-44 mg/dl, sugar-5 mg/dl, India Ink-negative, CSF for fungal culture revealed-Aspergillus fumigatus.


   Investigation Top



   Differential Diagnosis Top


Tuberculous meningitis, CNS toxoplasmosis.


   Treatment Top


By the end of June 2010, he was put on anti-retroviral therapy (stavudine-lamivudine-efavirenz) regimen.

Again he was admitted from 23/7/10 to 16/8/10. Considering his raised ADA and Cryptococcal antigen positive and positive HIV status, he was given both anti-tubercular treatment (T. Isoniazid 300 mg, T. Ethambutol 800 mg, T. Levofloxacin 750 mg, Note: patient showed rifampicin induced hepatitis) and added amphotericin-B.

His ATT was stopped in early February 2011.

In the middle of August 2011, ATT was started again.




   Discussion Top


CNS complications are the most dreaded complications in patients of HIV. It can be due to primary HIV infection itself or secondary to opportunistic infections. Some common opportunists that involve CNS are toxoplasmosis, cryptococcosis, progressive multifocal leukoencephalopathy, and primary CNS lymphoma. [1] Other less common problems include mycobacterial infections; syphilis; and infection with Cytomegalo Virus, Human T Lymphotrophic Virus-I, Trypanosoma cruzi, or Acanthamoeba. CNS aspergillosis in HIV is a rare complication. The primary risk-factors for invasive aspergillosis are profound neutropenia and glucocorticoid use; risk increases with longer duration of these conditions. [2] Neutrophil and/or phagocyte dysfunction is also an important risk-factor, as evidenced by aspergillosis in chronic granulomatous disease, advanced HIV infection, and relapsed leukemia. [3] Aspergillus infection is rare in HIV disease because of relatively intact phagocytic cell function. [4] Hematogenous dissemination to the brain is a devastating complication of invasive aspergillosis. Single or multiple lesions may develop. In acute disease, hemorrhagic infarction is most typical, and cerebral abscess is common. Rarer manifestations include meningitis, mycotic aneurysm, and cerebral granuloma. [5] Local spread from cranial sinuses also occurs. Post-operative infection occurs rarely and is exacerbated by glucocorticoids, which are often given after neurosurgery. The presentation can be either acute or subacute, with mood changes, focal signs, seizures, and decline in mental status. Cerebral granuloma can mimic a primary or secondary tumor. Magnetic Resonance Imaging is the most useful immediate investigation; unenhanced CT of the brain is usually non-specific, and contrast is often contraindicated because of poor renal function. [6] More than half of the patients with AIDS who develop Invaive Aspergillosis have either neutropenia, usually secondary to ganciclovir, or corticosteroid treatment as additional risk factors. [7] Nevertheless, some patients with Invasive AspergillosisA have no such risk factors, and this observation, combined with the fact that aspergillosis typically occurs in the setting of advanced HIV infection with < 50 CD4 cells/μL, indicates that HIV infection may represent an independent risk-factor for IA. [7],[8],[9]

In our case report, patient was treated with ATT and steroids for CNS tuberculosis previously. Use of steroids might have predisposed him for aspergillosis.

 
   References Top

1.Lanska DJ. Epidemiology of human immunodeficiency virus infection and associated neurologic illness. Semin Neurol 1999;2:105-11.  Back to cited text no. 1
    
2.Walsh TJ, Hier DB, Caplan LR. Fungal infections of the central nervous system: Comparative analysis of risk factors and clinical signs in 57 patients. Neurology 1985;35:1654-7.  Back to cited text no. 2
[PUBMED]    
3.Bodey GP, Vartivarian S. Aspergillosis. Eur J Clin Microbiol Infect Dis 1989;8:413-37.  Back to cited text no. 3
[PUBMED]    
4.Minamoto GY, Barlam TF, Vander Els NJ. Invasive aspergillosis in patients with AIDS. Clin Infect Dis 1992;14:66-74.  Back to cited text no. 4
[PUBMED]    
5.Woods GL, Goldsmith JC. Aspergillus infection of the central nervous system in patients with acquired immunodeficiency syndrome. Arch Neurol 1990;47:181-4.  Back to cited text no. 5
[PUBMED]    
6.Boes B, Bashir R, Boes C, Hahn F, McConnell JR, McComb R. Central nervous system aspergillosis. Analysis of 26 patients. J Neuroimaging 1994;4:123-9.  Back to cited text no. 6
[PUBMED]    
7.Khoo SH, Denning DW. Invasive aspergillosis in patients with AIDS. Clin Infect Dis 1994;19:S41-8.  Back to cited text no. 7
[PUBMED]    
8.Holding KJ, Dworkin MS, Wan PC, Hanson DL, Klevens RM, Jones JL, et al. Aspergillosis among people infected with human immunodeficiency virus: Incidence and survival. Adult and Adolescent Spectrum of HIV Disease Project. Clin Infect Dis 2000;31:1253-7.  Back to cited text no. 8
[PUBMED]    
9.Lortholary O, Meyohas MC, Dupont B, Cadranel J, Salmon-Ceron D, Peyramond D, et al. Invasive aspergillosis in patients with acquired immunodeficiency syndrome: Report of 33 cases. French Cooperative Study Group on Aspergillosis in AIDS. Am J Med 1993;95:177-87.  Back to cited text no. 9
[PUBMED]    

Top
Correspondence Address:
Sameer Saraf
Department of Medicine, King George Medical University, Lucknow, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.116493

Rights and Permissions



This article has been cited by
1 Rifampicin
Reactions Weekly. 2013; 1472(1): 33
[Pubmed] | [DOI]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Email Alert *
    Add to My List *


    Abstract
   Introduction
   Case Report
   Investigation
    Differential Dia...
   Treatment
   Discussion
    References

 Article Access Statistics
    Viewed1243    
    Printed56    
    Emailed0    
    PDF Downloaded16    
    Comments [Add]    
    Cited by others 1    

Recommend this journal